Spinal Cord Stimulation and Intraspinal Infusions for Pain

Indications and Specific Selection Criteria

The most common indication for SCS in the United States is for back or neck radiculopathic pain. Patients presenting with conditions such as lumbar or cervical radiculopathy, postlaminectomy syndrome, spondylolisthesis, spondylosis, or even persistent and refractory axial low back pain of uncertain etiology may respond to treatment with SCS and should be assessed. Topography of pain that is amenable to overlap by paresthesia of the spinal cord–stimulating device is a requirement for successful treatment. Radicular patterns tend to be more easily obtained than axial patterns, and for this reason, patients with pain predominantly in the extremities may be better candidates than patients with predominantly axial symptoms. This should not exclude a trial in an otherwise good candidate who has primarily axial symptoms. Although it is technically more difficult to obtain coverage of patients with predominantly axial back or neck pain, newer, more compact electrodes with multiple arrays sometimes placed bilaterally and triangularly might be useful in providing relief to patients with axial pain, and these arrays should be considered. Long-lasting relief is a reasonable goal. A large series of patients with follow-up of 2 to 20 years demonstrated that 52% of patients continued to have a 50% reduction in pain. The authors noted that even among patients who did not claim a 50% reduction of pain, most patients continued to use their devices.

The evidence of efficacy of SCS for back and neck pain is not lacking. A literature review was performed on studies of patients with SCS for chronic leg and back pain and included all relevant articles identified through MEDLINE search from 1966 through 1994. Fifty-nine percent of patients reported in these studies had greater than 50% pain relief at a time between 1 and 45 months after surgery. These authors noted the lack of a randomized trial at that time. Subsequent to this, a prospective, randomized comparison of SCS and reoperation in patients with persistent radicular pain with or without low back pain after lumbosacral spine surgery was conducted. The primary outcome measure of this study was frequency of crossover to the alternative procedure. This study showed a statistically significant advantage of SCS over reoperation. A literature review on SCS for chronic pain of spinal origin was conducted by North and Wetzel, who concluded that SCS is a valuable treatment option, particularly for patients with chronic pain of predominantly neuropathic origin and a topographic distribution involving predominantly the extremities. Efficacy may be better for spontaneous than for evoked pain.

Pain associated with spinal cord injury has been treated with SCS. Most authors report satisfactory responses in a smaller percentage of their patients ranging between 20% and 40%. Case reports supporting the use of SCS for whiplash and idiopathic acute transverse myelitis have been published. ^, Sindou and colleagues reported the predictive value of somatosensory-evoked potentials assessing neural conduction in the dorsal columns. These authors suggest that if central conduction time is abolished or significantly altered, then the success rate of SCS is dramatically less than in patients with normal preoperative central conduction times.

The usefulness of SCS for the treatment of postherpetic neuralgia has recently been described in a prospective case series involving 28 patients with either acute herpes zoster or postherpetic neuralgia studied over 29 months. Eighty-two percent of patients with intractable pain for longer than 2 years had a median decrease in their VAS score from 9 to 1 (0 to 10 scale) as well as improvement in their pain disability index. Four patients with acute herpes zoster had prompt and dramatic improvement in their pain symptoms.

The treatment of PVOD with SCS is the most common indication for this modality in Europe. For no other indication is the early evidence of efficacy more compelling and yet SCS for PVOD is not a common treatment in the United States. One study reported 37 patients receiving adequate pain relief after a trial in 41 patients with end-stage peripheral vascular disease. Seventy-eight percent of patients reported substantial pain relief at a mean follow-up of 25 months. Another investigator reported the results of SCS in 20 patients with ischemic rest pain and ulcers. Eighteen of 20 patients in this study had immediate relief of pain after electrical stimulation. These authors also reported improved skin nutritional flow leading to healing of ulcers of moderate size and increased salvage of feet with limb-threatening ischemia at 2-year follow-up. They report an increase in capillary density and an increase in red blood cell velocity and peak red blood cell velocity after arterial occlusion by intravital capillary microscopy.

More recently, SCS has been investigated by the European Peripheral Vascular Disease Outcome Study. Patients with nonreconstructable critical leg ischemia showed increased limb survival when compared with patients receiving usual treatment without SCS, as well as improved pain relief. Patients received an implant if their transcutaneous oxygen pressure measurement was 10 to 30 mm Hg before SCS trial or if it was less than 10 mm Hg but improved to 20 mm Hg or more during the SCS trial. Limb amputations were 20% at 12 months in the SCS group compared with 46% in the matched no SCS group. These and other authors suggest the routine use of transcutaneous oxygen pressure both before and during the trial phase as a predictor of success. A useful predictor of success in patients with diabetes with PVOD is the absence of autonomic neuropathy. Twenty-five of 28 patients with autonomic neuropathy failed SCS treatment, whereas all 32 patients without autonomic neuropathy had successful outcomes.

Evidence exists of the efficacy of SCS in severe Raynaud phenomenon and Buerger disease. SCS has shown remarkable effectiveness and should be considered as a treatment for patients with severe PVOD that is not amenable to surgical intervention.

Despite the lack of an identifiable objective lesion, SCS appears to be quite effective for treatment of CRPS. One report retrospectively reviewed experience with SCS and found 12 patients with CRPS who were followed up for an average of 41 months after implantation. Eight of these patients reported excellent pain relief, and four patients reported good pain relief. Another study looked at 18 patients with CRPS. Fourteen patients had a successful trial and subsequently had their systems internalized. Follow-up varied from 4 to 14 months. Six of 14 patients had good pain relief. Five had moderate pain relief. One had minimal and three had no pain relief. Of note is that pain relief was limited to the body parts covered by the paresthesia.

In a randomized trial comparing SCS plus physical therapy with physical therapy alone in 54 patients with CRPS, the SCS group had a mean reduction in pain of 2.4 cm (on a 1- to 10-cm scale) compared with an increase of 0.2 cm in the physical therapy alone group. Health-related quality of life also improved in the SCS group, but, interestingly, there was no difference between the groups in functional status.

A recent report has demonstrated that response to sympathetic blockade can be predictive of a better outcome from SCS for patients with CRPS. Thirteen of 13 patients with a positive response to sympathetic blockade had pain relief during the trial period, and 87% had greater than a 50% reduction in pain at 9 months. Only 3 of 10 patients with a negative response to sympathetic blockade had good relief and went on to permanent implantation, and only 33% had a 50% reduction in pain at 9 months.

It appears that at this time there are very good data to support the use of SCS for the treatment of CRPS if it is possible to obtain paresthesia coverage that overlaps the painful area.

The treatment of postamputation phantom or residual limb pain with SCS is still a controversial area. Contradictory reports for this and for brachial plexus avulsion injury pain exist, and it is not possible to make definitive recommendations for treating or not treating phantom limb or brachial plexus avulsion injury pain with SCS based on these data.

A large body of data supports the use of SCS for intractable angina pectoris. The complexity and implications of severe coronary artery disease as an indication for SCS requires discussion. The first published report of the use of SCS for angina was in 1987. These investigators described 10 patients with intractable angina in whom SCS devices were implanted, which led to a decrease in the frequency and severity of angina and a major reduction in the use of antianginal medications. Other investigators followed with a report on 10 patients and added bicycle ergometry as a measure of exercise tolerance and showed an increase in work capacity, increased time to angina, decrease in recovery time, and a decrease in the magnitude of ST segment depression associated with angina. By 1991, it was shown that reductions in angina attacks continued over 9 months, and a persistence in increase in rate-pressure product (a measure of the ability of the heart to do work). Between 1993 and 1994, results of a randomized, prospective study demonstrated improved exercise capacity, improved quality of life, and a decrease in ischemic episodes as measured by Holter monitor. Complications were few and of a technical nature, and a surgical algorithm that did not involve a trial before implantation was described. It has been shown that SCS does not conceal myocardial infarction that may occur in patients with implanted devices. A decrease in hospital admissions for patients with implanted SCS devices compared with a control group has been demonstrated. In 80% of patients, the beneficial effect has been reported to last 1 year, and in 60%, improvement in exercise capacity and quality of life lasted as long as 5 years. There are no data showing harmful or nontherapeutic effects of SCS for angina. The use of SCS may be beneficial even in critically ill patients. Janfaza and colleagues reported the 6-week survival in such a patient, whereas other investigators have reported an effect insufficient to overcome the severity of ischemic disease, albeit relief of ischemic symptoms, until death occurred.

A prospective, randomized trial of SCS versus coronary artery bypass grafting in 104 patients with severe angina, increased surgical risk, and no prognostic benefits from revascularization demonstrated long-lasting improvement in quality of life and comparable survival and symptom control in both groups. Benefit after discontinuation of SCS has been shown for as long as 4 weeks after discontinuation. No difference in anginal complaints, nitroglycerin intake, ischemia, or heart rate variability was shown. SCS has been shown to decrease hospitalization in patients with angina, and there is evidence that modern SCS devices are compatible with modern pacemaking devices. ^,

Description of Technique

In our practice, patients who meet selection criteria are instructed not to eat or drink anything after midnight the night before their implantation trial. They are instructed to continue their nonsteroidal antiinflammatory drugs, but care is taken to discontinue other anticoagulants or platelet inhibitors for proper durations of time. The procedure is done in two stages. Both the trial phase (phase 1) and the generator implantation phase (phase 2) are done in the operating room with an anesthesiologist present. The trial phase (phase 1) involves either the placement of a percutaneous cylindrical electrode or a paddle-type electrode placed via minilaminectomy. The electrodes are either removed after a period of trial stimulation or are attached to a connecting cable during phase 1, allowing the electrode to remain under the skin entirely. In this case, the connecting cable can be removed and the electrode attached to a new sterile cable during phase 2.

Patients with chronic pain may have central changes that amplify painful signals. It is necessary to have the patient awake and able to answer questions appropriately to assess the location of paresthesia during the trial phase. Patients may require laminectomy for placement of a paddle-type electrode in the thoracic or cervical region. Patients with chronic pain often have multiple comorbidities, particularly patients with PVOD or intractable angina pectoris. These factors create an anesthetic challenge and require a preoperative consultation between surgeon and anesthesiologist to define goals and needs. Our typical anesthetic involves intravenous fentanyl and midazolam for analgesia, anxiolysis, and amnesia and propofol for sedation. The propofol can be turned off and the patient awakened for questioning regarding paresthesia topography at appropriate intervals. We also use large volumes of local anesthetic, typically 0.5% lidocaine without epinephrine. A dose of 4 mg/kg (56 mL for a 70-kg person) can be safely administered even as a single dose and more can be administered after 1 or 2 hours. Another option is intravenous remifentanil plus local anesthetic, but this requires an anesthesiologist experienced in the use of this drug because the therapeutic window is often so narrow. Despite the best efforts of experienced practitioners, the implanter should be prepared for oversedation and the need for airway control during the procedure or suboptimal ability to describe the paresthesia topography ( Video 120.1 ). The patient should be advised that this is a possibility and that if it occurs, the electrode can still be placed without paresthesia guidance, but success rate might be reduced. The patient should also be educated about information needs that will occur intraoperatively before getting to the operating room. A recent report describes the successful implantation of an SCS device in 19 of 19 patients undergoing laminectomy with 12.5- to 20-mg bupivacaine intrathecal spinal anesthesia. In all patients with spinals and anesthesia throughout the surgical procedure, SCS paresthesia was readily appreciated by the patients.

There is no description of the absolute need for alertness and ability to communicate during surgery. It is generally accepted that, due to uncertainty about anatomic and physiologic overlap, simply placing the lead at the proper anatomic location will not reliably produce a paresthesia that will be effective in reducing pain. There are published case series in which successful implantation has been done under general anesthesia.

A retrospective, nonrandomized review of surgical experience concluded that patients with flat electrodes placed via laminectomy had better pain relief that was longer lasting than patients who had percutaneously placed cylindrical electrodes. A prospective, randomized, controlled trial has recently shown that electrode arrays implanted via laminectomy had lower amplitude requirements and better patient ratings of paresthesia coverage. The decision as to whether to place a flat electrode via minilaminectomy or a percutaneously placed cylindrical electrode is a controversial and emotionally charged issue because anesthesiologists, who place most of these devices, use a percutaneous approach and many neurosurgeons place leads via laminectomy. To further complicate matters, anesthesiologists should not place leads via laminotomy because they do not have the training, experience, or ability to manage complications and many pain specialist anesthesiologists derive substantial income from placing SCS devices (see Video 120.1 ). In addition, other specialists such as physiatrists and neurologists are receiving training and are eligible for board certification in pain medicine and are implanting cylindrical leads. At this time, there is no overwhelming evidence of the advantage of placing electrodes via a laminectomy compared with percutaneously placed leads, but there is at least one compelling study.

For percutaneous placement of a cylindrical electrode, the procedure is as follows. Patients are placed prone on a fluoroscopy table in the operating room and prepared for a surgical procedure that can last hours. We do not place a Foley catheter. Standard surgical preparation is done after identifying important landmarks fluoroscopically and marking the skin to identify them. The skin and subcutaneous tissue are anesthetized with local anesthetic before insertion of the 15-gauge epidural needle. The epidural space is identified using a loss of resistance to air or saline technique ( Fig. 120.1 ). For a patient with an L5 radiculopathy pain pattern, the epidural space is entered at approximately T12–L1, at which point the cylindrical electrode is advanced through the needle and positioned using fluoroscopic guidance to the desired level at approximately T9–T10, at which time trial stimulation is carried out ( Figs. 120.2 and 120.3 ) . For placement of a device for stimulation of the upper extremity, entry is made at T1–T3 with the electrode tip to arrive at C3–T4 approximately. The target site for the electrode tip for a patient with angina is approximately T4–T5. For a unilateral syndrome, the electrode should be positioned approximately 3 mm ipsilaterally off midline. The electrode can be directed and “steered” using an angled stylet. Once the target anatomic site is reached, the electrode is anchored and attached to a temporary screening cable and a trial screener. The awakened patient is then questioned about the presence or absence and location of paresthesia coverage. Parameters that are available for adjustment include amplitude and pulse width and frequency, the same as with an implanted generator (see Video 120.1 ).

Once good paresthesia overlap to pain topography is obtained, the electrode is disconnected from the cable. A 5-cm vertical incision over the site of epidural needle placement is made. The subcutaneous tissue is undermined at the level of the lumbodorsal or supraspinous fascia, the epidural needle is carefully removed along with the electrode stylet, and the lead is anchored using an anchoring device that will prevent the electrode from migrating ( Fig. 120.4 ). The electrode is attached to a percutaneous extension lead, and a tunneling device is used to exit the skin at a site approximately 10 cm lateral to the incision. The electrode is placed within the incision with only the temporary connecting cable externalized. This allows the electrode to remain beneath the skin throughout the entire trial period. Care should be taken to avoid contact of the electrocautery device with the electrode. A defect in the electrode could result in a line of continuity between the externalized lead and the epidural space. If the patient has a successful trial, then it is necessary to remove only the extension lead, and the electrode, which has already been positioned and has not been exposed to a contaminated external environment, can remain in place. The skin and subcutaneous tissue are closed with interrupted Vicryl sutures and skin staples (see Video 120.1 and 120.2).

Placement of a paddle-type electrode or flat lead is done via a standard laminotomy procedure. The electrode is placed in the epidural space using the same anatomic targets as described for cylindrical electrode placement. A dual laminotomy is sometimes required to properly position the electrode. Paresthesia overlap with topography of pain should be tested with the awake patient intraoperatively. The electrode cable is anchored to fascia, and the electrode is attached to a temporary percutaneous connecting wire as described previously.

At the conclusion of the phase 1 of implantation, the procedure is the same for both percutaneous and flat electrode management. The percutaneous connecting cable is attached to a trial screener, and the patient is screened at home for 4 to 7 days. When the patient returns, he or she is questioned about success of pain reduction. A general rule of thumb is that a reduction in pain of 50% or more is necessary to proceed to phase 2, but there are many exceptions and a careful assessment by the implanting surgeon is required for proper decision-making. For patients with intractable angina pectoris, a reduction in the frequency, intensity, and duration of anginal episodes should be documented.

For phase 2, the patient is taken to the operating room, and under local anesthesia with monitored anesthesiology care, the electrode and cable are removed if the trial was not successful. Patients who have had a successful trial will have their incision reopened, and the generator will be implanted in the buttock. A site selected below the belt line and cephalad enough to allow comfortable sitting should be selected. Generators can be implanted in a variety of anatomic sites, including the abdomen, lateral thorax, and subclavicular and subaxillary space.

After local anesthetic infiltration, a horizontal incision is made in the skin planes large enough to enable placement of the generator. The pocket is created by sharp and blunt dissection and is made at a depth no greater than 2 cm to enable easy programming transcutaneously.

A tunneling tool is used to connect the midline incision to the pocket, and the extension wire is threaded through the tunnel. The system is connected, and the incisions are approximated in two layers using 3-0 Vicryl sutures for the deeper tissues and staples for skin closure. Familiarity with all the equipment is necessary before proceeding to the operating room.

Intraoperative problems peculiar to SCS implantation include an inability to properly position the electrode in the epidural space, inability to obtain paresthesia overlap of the painful area, and unanticipated events. We have described the inability to thread a percutaneous catheter in a patient with unidentified epidural lipomatosis. The catheter was readily placed under direct vision after laminotomy. We use a dual laminotomy technique in those cases in which a proper anatomic position cannot be achieved through a single laminotomy to enable proper anatomic and physiologic positioning of a flat electrode and have estimated that unanticipated anatomic complications occur as often as 18% of the time in revision flat electrode placements. Finally, it is uncommon, but it is sometimes impossible to obtain satisfactory paresthesia overlap of the painful area, particularly with angina pectoris and axial low back or neck pain, despite an unimpeded ability to manipulate the electrode(s). Even distal extremity paresthesia coverage can sometimes be impossible to obtain for unproven but theorized reasons such as epidural scarring or any impediment to the flow of electricity to and into the spinal cord.